Zinc deficiency among human populations, once thought to be exceedingly rare, has recently gained attention as a potential public health problem of major import. Among those physiologically stressed groups at greatest risk of developing zinc deficiency are pregnant and lactating women and their rapidly growing infants and children. Investigation regarding the zinc nutriture of lower animals has disclosed that zinc deprivation during gestation, even if transitory, is terotogenic, affecting development of nearly every organ system. Animals deprived of zinc postnatally show markedly retarded growth, particularly that of lymphoid tissue, and may have an increased risk of latent disabilities, e.g., learning disorders. To address these issues in a model more relevant to the human, we will serially study pregnant and lactating mothers and neonatal non-human primates maintained on either marginally zinc deficient or control diets. At defined intervals, maternal animals will be monitored for anthropometric, clinical biochemical, endocrine, and immunohematological parameters; anthrometric, clinical biochemical, endocrine, immunohematologic, cytogenetic, pulmonary, and behavioral characteristics of offspring will be monitored. At the time of weaning, zinc deficient infants will be fed either a continuation of zinc-deprived diet or switched to an ad libitum-fed control regimen, thereby enabling us to address the issue of neonatal lesion reversibility. The association between zinc deprivation and anomalous development in humans is a problem of growing concern, and both the mechanism of action and the clinical features, as well as the potential long-term significance of this syndrome must be more clearly defined and characterized.